【Abstract】　Objective　To quantify the burden of Borrelia burgdorferi in different representative tissues from the murine host  by real time quantitative PCR(Q-PCR). Methods　Low-passage B.burgdorferi was cultivated to logarithmic growth phase, and diluted to a concentration of 1×10⁵/ml for experimental use. To establish a B.burgdorferi-infected murine model, mice were injected 100 μl diluted culture intradermally in the back. After artificial infection was confirmed, mice were sacrificed at 12 d and 18 d post-infection in CO₂ box. Samples from skin, joint, heart and urine bladder were collected aseptically and frozen at -80 ℃, and total DNA was extracted. B.burgdorferi flaB was quantified by Q-PCR. Data were analyzed statistically to determine if bacterial burdens in various tissues showed a significant difference. Results　spirochete burden was the highest in the urine bladder, medium in the skin and joint, lowest in the heart.  Conclusion　There was significant difference among spirochete burden in various tissues. Spirochete burden in the tissue was not positively related to the severity of this tissue.

Lyme borreliosis is a prevalent arthropod-borne disease caused by the spirochete, Borrelia burgdorferi. The microbe consists in nature through an intricate tick-mammal cycle. B.burgdorferi is transmitted to vertebrates via ticks belonging to the Ixodes ricinus complex. Over the last two decades, scientists have been trying to unravel the complex mechanisms by which B.burgdorferi maintained in a unique enzootic cycle. Our special attention has been paid to addressing the molecular interaction strategies that B.burgdorferi employs for effective colonization, migration and transmission through ticks. Studies have shown that B.burgdorferi expresses a select set of genes in distinct phases of its life cycle- and in specific tissue locations. The outer surface protein (Osp) A of B.burgdorferi is down-regulated within a mammalian host, turned on as soon as the spirochete enters and resides in the arthropod vector. OspA acts as an adhesion, which binds a receptor in the tick midgut, and OspA is required for spirochetes to successfully colonize in the tick midgut. B.burgdorferi lacking OspA cannot survive in the tick. To further understand the mechanism of OspA-based adherence, we have recently identified and characterized the tick receptor for OspA, named TROSPA. TROSPA predominantly localized in the tick midgut, specifically bound to ospA expressing B.burgdorferi and TROSPA knockdown ticks allowed poor attachment of spirochetes in the tick midgut. These observations clearly indicate that like OspA, TROSPA is also actively engaged in the colonization of spirochetes in Ixodes ticks. The OspA-TROSPA interaction is the first illustration of a molecular interface where both microbial as well as vector gene products equally contribute to B.burgdorferi survival in nature. We also find that there are the complex pathogen-vector-mammalian host triangle interactions during mammalian infection tith B.burgdorferi. Ixodes tick salivary protein Salp15 help spirochetes to infect the mice. B.burgdorferi basic memrane protein A gene(bmpA) andbmpB facilitate spirochetes to disseminate to and locate in joint tissue and induce arthritis. All these findings provide deep insights into transmission and pathogenesis of B.burgdorferi.